Evidence that release of adenosine triphosphate from endothelial cells during increased shear stress is vesicular
Evidence that release of adenosine triphosphate from endothelial cells during increased shear stress is vesicular
复制标题
DOI：
10.1097/00005344-200112000-00012
复制
发表时间：
2001-12-01
影响因子：
3
通讯作者：
Burnstock, G
中科院分区：
文献类型：
--
作者：
Bodin, P;Burnstock, G
为了应对剪切应力的增加，血管内皮细胞通过未知的机制释放三磷酸腺苷（ATP）。我们使用不同的方法研究了这种机制。首先，我们发现了奎纳克林，用于定位与肽结合的 ATP 的细胞内储存。显示出典型的囊泡储存的颗粒状荧光。第二。我们发现，两种囊泡运输抑制剂（莫能菌素和 N-乙基马来酰亚胺）可显着减少血管内皮细胞响应剪切应力增加而释放的 ATP。使用囊性纤维化跨膜调节剂抑制剂的初步实验。磺酰脲类受体。多药耐药蛋白显示这些 ATP 结合盒转运蛋白（先前在内皮细胞中的特征）不参与 ATP 释放机制。因此，我们认为血管内皮细胞（如神经细胞）可能通过囊泡胞吐作用释放 ATP。
In response to increased shear stress, vascular endothelial cells release adenosine triphosphate (ATP) by an unknown mechanism. We have investigated this mechanism using different approaches. First, we discovered that quinacrine, used to locate intracellular stores of ATP bound to peptides. displayed a granular fluorescence, typical of vesicular storage. Second. we found that two inhibitors of vesicular transport (monensin and N-ethylmaleimide) produced a highly significant reduction in the release of ATP from vascular endothelial cells in response to increased shear stress. Preliminary experiments using inhibitors of the cystic fibrosis transmembrane regulator. the sulfonylurea receptor. and the multidrug resistance protein showed no involvement of these ATP-binding cassette transporter proteins (previously characterized in endothelial cells) in the mechanism of release of ATP. We suggest, therefore, that the release of ATP from vascular endothelial cells, like that of nerve cells, is probably by vesicular exocytosis.